• In subaorticstenosis
– Gradient is between the main portion of the left ventricle and its outflow
tract, although in tunnel subaortic stenosis there may be no discrete
subvalvular chamber.
• In supravalvular stenosis
– Gradient is just beyond the aortic valve, between the initial segment of the
proximal aorta (just beyond the aortic valve) and the main segment of the
ascending aorta.
– To facilitate surgical intervention, it is important to identify the site and
nature of the obstruction in each instance.
– This is determined by both hemodynamics and angiography
• The left ventricle becomes progressively hypertrophied in aortic
stenosis.
• The cardiac output is well maintained until the left ventricle dilates
and fails; it then becomes progressively reduced.
4.
Pathophysiology
• LV outflowobstruction
– increased LV systolic pressure
– increased LV ejection time (LVET)
– increased LV diastolic pressure
– decreased aortic (Ao) pressure.
• Increased LV systolic pressure with LV volume overload
– increases LV mass LV dysfunction and failure.
• Increased LV systolic pressure, LV mass, and LVET
– increase myocardial oxygen (O2) consumption.
• Increased LVET
– decrease of diastolic time (myocardial perfusion time).
• Increased LV diastolic pressure and decreased Ao diastolic pressure
– decrease coronary perfusion pressure.
• Decreased diastolic time and coronary perfusion pressure
– decrease myocardial O2 supply.
• Increased myocardial O2 consumption and decreased myocardial O2 supply
– myocardial ischemia, which further deteriorates LV function
5.
• The normaladult aortic valve area –
– between 3.0 and 4.0 cm2
.
• When aortic valve disease is present, the aortic
velocity depends on the size of the valve orifice
and transaortic volume flow.
• A normal cardiac output can be maintained
without a significant increase in aortic velocity
until valve area is reduced to approximately
25% to 30% of normal.
6.
• In adults
–outflow obstruction usually develops and
increases gradually over a prolonged period
• In infants and children with congenital AS
– the valve orifice shows little change as the child
grows, thereby intensifying the relative
obstruction gradually
7.
• With decreasesin valve area below 1 cm2
, very
small changes in orifice area lead to marked
changes in transvalvular pressure gradient and
hemodynamic load.
• LV systolic pressure increases in proportion to the
severity of valve obstruction, with the potential
energy in the difference between LV and aortic
pressure converted into kinetic energy as blood is
ejected at high velocity across the valve
9.
Bernoulli equation
• Thevelocity (V) in the stenotic orifice correlates with
the drop in pressure (P) from the LV to the aorta
P = 4V2
• Relationship between instantaneous velocity and
pressure measurements at any point in systole.
• The mean systolic pressure gradient
– by averaging pressure gradients over the systolic ejection
period
10.
• The cross-sectionalarea of the open aortic
valve in systole is a robust measure of stenosis
severity. For a given aortic valve area, the
aortic velocity and pressure gradient will vary
with transaortic volume flow. To account for
transaortic volume flow rate, aortic valve area
(AVA) can be calculated based on the
continuity principle
11.
Continuity principle
• Thestroke volume (SV) in the aortic valve (AV) orifice
and the stroke volume just proximal to the valve in the
LV outflow tract (LVOT) are equal:
– SVAV = SVLVOT
• Stroke volume
– SV = CSA x VTI
• Thus the Continuity equation can be solved for aortic
valve area:
– AVA x VTIAV = CSALVOT x VTILVOT
– AVA = (CSALVOT x VTILVOT)/VTIAV
12.
• The standardclinical hemodynamic parameters of
aortic stenosis
– Transaortic velocity
– Mean transaortic pressure gradient
– Aortic valve area
• Others
– LV stroke work loss
– Recovered pressure gradient
– Energy loss index
– Valvuloarterial impedance
16.
• Aortic stenosis increased pressure load on the LV
compensatory LV hypertrophy maintains normal wall
stress
– Wall stress is proportional to LV pressure (P) and radius (r) and
inversely related to wall thickness (Th):
• σ = (P x r)/2Th
• Concentric hypertrophy
– additional sarcomeres aligned in parallel with a corresponding
increase in cardiac myocyte size.
– increase in interstitial tissue with fibrosis, which contributes to the
long-term diastolic dysfunction
18.
• LV hypertrophy
–diastolic dysfunction and increased dependence on
the atrial contribution to LV filling
– atrial fibrillation may precipitate symptoms of heart
failure due to a combination of increased LV filling
pressures and decreased forward cardiac output.
• LV ejection fraction and wall stress remain
normal due to LV compensatory mechanisms to
increase wall thickness
20.
• The increasein afterload may eventually
exceed the compensatory LV response
• afterload mismatch
• Impaired LV systolic function
21.
Afterload mismatch
– Preservationof myocardial contractile function,
but impaired systolic function due to high
afterload
– LV systolic function should improve if afterload is relieved
with replacement of the stenotic valve
– average improvement
• 10 ejection fraction units
Cardiac catheterization
• Whennoninvasive data are nondiagnostic
• If there is a discrepancy between clinical and
echocardiographic evaluation
25.
Correlation between clinicalseverity of AS
and aortic valve area
AVA Clinical severity
>1 Mild (Symptoms rare in the absence of other heart disease)
0.7-1 Moderate (Symptoms with unusual stress, AF,Exercise etc)
0.5-0.7 Moderately severe(Symptoms with activities of daily living)
<0.5 Severe(Symptoms at rest or minimal exertion, biventricular failure)
26.
• In thehemodynamic assessment of valvular aortic stenosis, primary
importance should be placed on obtaining simultaneous
measurement of pressure and flow across the aortic valve,
whichpermits calculation of the aortic orifice or valve area (AVA).
• In the typical adult with symptomatic aortic stenosis, AVA is reduced
to < / = 0.7 cm2
.
• Occasionally, a valve of 0.8 to 0.9 cm2
results in a symptomatic
presentation, especially when there is concomitant coronary artery
disease or hypertension or when the absolute value of cardiac
output is high (e.g., a large patient, anemia, fever, or thyrotoxicosis).
• When AVA is </=0.5 cm2
, severe aortic stenosis is present and
cardiac reserve is minimal or absent
27.
Catheterization Protocol
• Rightheart catheterization for measurement of right heart pressures and cardiac output.
• Left heart catheterization for measurement of pressure gradient across aortic valve and
LVEDP and assessment of the presence or absence of a transmitral gradient (concomitant
mitral stenosis)
– Approach
• Brachial – Sones catheter
• Brachial /Radial – MP catheter
• Femoral – Pigtail
• Left ventriculography
– the stenotic orifice of the valve during systole as outlined by a jet of contrast material ejected
into the aorta.
– The valve cusps may appear irregular, their mobility may be reduced, and often the number of
cusps can be identified
– In congenital aortic stenosis, the valve may form a funnel during systole.
– The ascending aorta is dilated (poststenotic dilatation), but the subvalvular area is widely patent.
– A subaortic membrane, with a small central orifice, or a subvalvular muscular ring may be seen.
– The characteristic changes of idiopathic hypertrophic subaortic stenosis may be observed.
– In supravalvular stenosis, the narrowing of the proximal aorta can be seen
29.
Aortography
• In pureaortic stenosis, aortography often demonstrates
a negative jet of radiolucent blood exiting focally from
the left ventricle.
• In the patient with aortic stenosis who also has some
aortic regurgitation, aortography permits a rough
quantitation of the severity of the regurgitation.
• If interventional catheter techniques (e.g., balloon aortic
valvuloplasty) are under consideration, determination of
the extent of associated aortic regurgitation may
become important in clinical decision making.
30.
Prussian Helmet sign
•In congenital aortic
stenosis, there may be
upward doming of the
aortic valve leaflets,
which together with the
central negative jet
gives the so-called
Prussian helmet sign.
31.
Assessment of stenosisseverity
• Measurement of the pressure gradient
• Analysis of the pressure waveforms
• Measurement of cardiac output
• Calculation of the valve area
• Angiocardiography of the chamber upstream
to the site of stenosis
33.
Pressure gradient
• Describedby three invasive measurements:
– The mean gradient
– The peak-to-peak gradient
– The maximum gradient.
• The mean and maximum gradients are used to evaluate stenosis
severity
• The rate of rise of LV pressure (dP/dt) during isovolumic
contraction provides a relatively loadindependent measure of LV
systolic function
35.
Pressure-Volume Loops
• bygraphing instantaneous pressure (on the vertical axis)
against volume (on the horizontal axis).
• LV stroke volume
– the distance on the horizontal axis between end-diastole and end-
systole
• LV stroke work (the integral of pressure times volume over the
cardiac cycle)
– the area enclosed by the pressure-volume loop.
• Elastance or Emax
– the slope of the end-systolic pressure-volume relationship under
different loading conditions provides a load-independent measure of
LV systolic function
Normal Values atCardiac Catheterization
(Supine, Resting Adults)
43.
Catheters & Techniques
•Wires and catheters
– 0.038-inch standard straightwire
– pigtail catheter, Judkins right, or Amplatz left
– Feldman catheter & Rosen wire – specifically designed to cross aortic valve
– Double lumen pigtail
• Supravalvular angiography
– When staright wire does not cross
– useful to localize the position and orientation of the valve orifice
• The position and movement of calcium within the valve leaflets may
also suggest the location of the valve orifice.
• Hydrophilic straight wires
– wire coating may increase the risk for valve leaflet perforation.
44.
• Probing theaortic valve orifice with the wire should be done in
less than 2-minute increments, with the wire removed and the
catheter carefully flushed prior to reinsertion and another
attempt to cross the valve
• Risk of Neurologic insult
– 3% - clinically significant neurologic event
– 22% - magnetic resonance imaging evidence of an acute cerebral
embolic event.
• Transseptal puncture
– Severe aortic valve calcification
– Critical AS
– Coexisting mitral stenosis
45.
Pressure gradient
• (1)The mean gradient
• (2) The peak-to-peak gradient
• (3) The maximum gradient
46.
• Five invasivemethods can be used to measure
pressure gradients between the left ventricle
and the aorta
• The single-catheter “pullback technique”
• Simultaneous measurement of the proximal
aortic and the LV pressures using two
transducers yields the most accurate data.
47.
1st
method
• Single arterialpuncture
• 6 French sheath within the femoral artery
• Advancement of a 6 French double-lumen
catheter (Langston dual-lumen catheter, Vascular
Solutions, Minneapolis, MN) into the left ventricle
• Simultaneous measurement of the aortic and LV
pressures
• Following measurement of the gradient, a left
ventriculogram is done
48.
2nd
method
• Two arterialpunctures
• One catheter positioned within the left
ventricle
• Second catheter located within the ascending
aorta
49.
3rd
method
• Venous puncture– Femoral vein
– To allow transseptal puncture
– Catheter is advanced from the left atrium into the
left ventricle
• Arterial puncture
– Second catheter positioned into the ascending
aorta
50.
4th
method
• Single arterialpuncture
• Standard, short 6 French sheath within the femoral artery
• 4 or 5 French pigtail catheter (through the 6 French sheath) into
the left ventricle
• The femoral artery pressure
– measured via the side-arm of the sheath
– used as a surrogate to the central aortic pressure
• With realignment –
– Gradient is underestimated by approximately 10 mm Hg
• Without realignment –
– Gradient is overestimated by approximately 9 mm Hg
• Therefore, the central aortic pressure should be measured for
accuracy
5th
method
• Single arterialpuncture
• Long (55 or 90 cm) 6 French sheath into the
ascending aorta with a smaller 4 or 5 French
sheath advanced through the long sheath into
the left ventricle
• The side-arm of the long sheath is used to
measure the central aortic pressure
54.
Newer method
• Bertoget al
• Single arterial puncture
• 4 French catheter into the ascending aorta
• LV pressure is measured using a 0.014-inch
pressure wire (placed through the 4French
catheter)
• Correlation with traditional methods was
excellent
55.
Analysis of pressurewaveform
• Without AS
– the slope and magnitude of the aortic and LV systolic
pressures are similar
– rise together to a midsystolic peak.
• With AS
– the pressure in the aorta rises slowly and achieves a late
systolic peak
• LV hypertrophy limits the ability of the left ventricle
to fill at a normal pressure, resulting in a higher end-
diastolic pressure.
57.
Carabello sign (1987)
•A rise in arterial blood pressure
during left heart catheter
pullback in patients with severe
aortic stenosis
• Catheter pullback showed
increases in peripheral arterial
pressure of 5 mm Hg in 15 of 42
patients.
• Fifteen of 20 patients (75%) with
AVA of 0.6 cm2
demonstrated this
phenomenon
• None of 22 patients with AVA of
0.7 cm2
showed such an increase.
58.
Cardiac output
FICK TECHNIQUE
•Oxygen serves as the “indicator”
• The uptake or release of oxygen
by a tissue is the product of the
amount of oxygen delivered to
the tissue times the difference in
oxygen content between the
blood entering and the blood
leaving thetissue
THERMODILUTION METHOD
• A known volume of cold saline is
injected into the right atrium
while a thermistor in the
pulmonary artery continuously
records temperature .
• Cardiac output is then calculated
from the known temperature (T)
and volume (V) of the injectate,
and the integral of temperature
over time (ΔT/dt) in the
pulmonary artery
Torricelli's law
• Firstformula
• flow across a round orifice
• F = flow rate
• A = orifice area
• V = velocity of flow
• Cc = coefficient of orifice contraction.
– The constant Cc compensates for the physical phenomenon that,
except for a perfect orifice, the area of a stream flowing through an
orifice will be less than the true area of the orifice.
64.
• Second principle
–relates pressure gradient and velocity of flow according to Torricelli's
law
– V =velocity of flow
– Cv=coefficient of velocity
• correcting for energy loss as pressure energy is converted to kinetic or velocity
energy
– H=pressure gradient in cm H2O
– g =gravitational constant (980 cm/sec2
) for converting cm H2O to units
of pressure
65.
• Combining the2 eqns
• C =an empirical constant accounting for CV and
CC
• h =in mm Hg
66.
• The diastolicfilling period
– begins at mitral valve
opening and continues
until end-diastole.
• The systolic ejection
period
– begins with aortic valve
opening and proceeds to
the dicrotic notch or other
evidence of aortic valve
closure
• Planimeter aortic-LVpressure gradients (area
= 12.2 cm2
) and measure systolic ejection
periods (SEPs = 4.1 cm).
• Next convert cm to time and convert
planimetered area to mean systolic pressure
gradient.
• Systolic ejection period of 4.1 cm/beat at
paper speed of 100 mm/s = 0.41 s/beat.
70.
• Mean valvegradient (MVG) = (area x scale
factor)/SEP (Scale Factor: 1 cm = 19.6 mm Hg)
• Aortic valve flow
• As heartrate increases during exercise, the systolic
ejection period tends to become shorter, but the
tendency is counteracted by both increased venous return
and systemic arteriolar vasodilation, factors that normally
help to maintain LV stroke volume constant during
exercise.
• The heart rate is increasing but the systolic ejection period
is diminishing only slightly so that their product (systolic
ejection time per minute) increases.
• This is the counterpart of the decreased diastolic filling
time per minute during exercise
75.
• With decreasingheart rate, the gradient increases in
aortic stenosis for any value of cardiac output.
• This is opposite to the effect of heart rate in mitral
stenosis and reflects the opposite effects of heart
rate on systolic and diastolic time per minute.
• As the heart rate slows in aortic stenosis, the stroke
volume increases if cardiac output remains constant.
• Thus the flow per beat across the aortic valve
increases and so does the pressure gradient
Pressure recovery
• Downstreamfrom the orifice, the flow stream expands and decelerates
with a corresponding decrease in kinetic and increase in potential
energy, a phenomenon called “pressure recovery”
• The net P between the LV and the mid-ascending aorta is lower than
the pressure drop immediately adjacent to the valve
• Doppler measures velocity at the narrowest orifice, thus Doppler Ps are
higher than the net P .
• The clinical impact of pressure recovery usually is small but can be
significant with mild stenosis and a small aortic root or with a doming
congenitally stenotic valve
79.
• In calculatingaortic valve area, the gradient between
sites 1 and 3, which records gradient before pressure
recovery, is probably the most accurate reflection of
the pressure drop across the valve.
• When the aortic catheter is placed at a more distal
site, it records the effect of pressure recovery, which
reduces gradient as blood flow again becomes laminar.
• The more proximal aortic position is probably the ideal
location for measuring the gradient for the valve area
calculation
80.
limitations of theGorlin-derived orifice area
• As the square root of the mean gradient is
used in the Gorlin formula, the valve area
calculation is more strongly influenced by the
cardiac output than the pressure gradient
81.
• Transducer Calibration
•Pullback Hemodynamics
– An augmentation in peripheral systolic pressure of
more than 5 mm Hg at the time of LV catheter
pullback indicates that significant aortic stenosis is
present. This sign is present in >80% of patients
with an aortic valve area of 0.5 cm2
or less
82.
Hakki’s formula
• Theproduct of heart rate, SEP or DFP, and the
Gorlin formula constant was nearly the same
for all patients whose hemodynamics were
measured in the resting state, and the value of
this product was close to 1.0
83.
Valve resistance
• Helpsto separate patients with severe aortic stenosis
from those patients who had similarly small calculated
aortic valve areas, but who were subsequently
demonstrated to have mild disease.
• Resistance appears less flow dependent than valve area
• Resistance is unlikely to supplant the Gorlin formula in
assessing stenosis severity, but may be an important
adjunct to it in patients with low cardiac output.
84.
• Resistance alsohas been shown to be more constant under
conditions of changing cardiac output than valve area.
• Resistance thus necessarily has a close relationship to valve area.
• Resistance rises sharply below a valve area of 0.7 cm2
.
• The shoulder of this curve is between 0.7 and 1.1 cm2
, which is the
common area of indeterminate significance of Gorlin aortic valve
area. Some patients in this gray zone tend to have higher valve
resistance than others.
• The patients with resistance >250 dynes x s x cm–5
are more likely to
have significant obstruction, whereas those with resistance below
200 dynes x s x cm–5
are less likely.
• Valve resistance is not expected to remain consistent.
• Dobutamine ornitroprusside
– for patients with a cardiac output of <4.5 L/minute who have a
transvalvular gradient of <40 mm Hg and a valve resistance of <275
dyn sec/cm-5
.
• If patients respond by substantially increasing the measured
gradient, they probably have truly severe aortic stenosis and
may benefit from aortic valve
replacement.
• If cardiac output increases substantially but gradient increases
only slightly or actually declines, the aortic stenosis is mild and
the patient is unlikely to benefit from aortic valve replacement
90.
True Vs. PseudoAS
• Obtain baseline measurements of cardiac output, heart
rate, and simultaneous LV and aortic pressures
• Initiate dobutamine by continuous infusion at 5 μg/ kg/min
• The dose is increased by 3 to 10 μg/kg/min every 5
minutes until a maximum dose of 40 μg/kg/min is
achieved
• The mean gradient increases to more than 40 mm Hg,
cardiac output increases by 50%, heart rate increases to
more than 140 beats per minute (bpm), or intolerable
symptoms or side effects (arrhythmias) occur.
• Patients withtrue, severe AS
– (1) mean aortic valve gradient greater than 30 mm Hg
– (2) an aortic valve area remains 1.0 cm2 or less
• Patients with pseudo–aortic stenosis
– (1) cardiac output increases
– (2) mean aortic valve gradient remains less than 30
mm Hg
– these findings indicate a component of a primary
cardiomyopathy and mild to moderate AS.
96.
Angiocardiography
• Left ventriculography
–should be routinely performed
– provides assessment of
• LV systolic function
• the anatomy of the aortic valve
• coexisting mitral regurgitation
• The aortic valve should be assessed for
– Calcification
– Leaflet morphology (bicuspid)
– leaflet mobility.
• A bicuspid aortic valve may show systolic doming of the
leaflets.